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Immunity
Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis
Skin barrier dysfunction, a defining feature of atopic dermatitis (AD), arises from multiple interacting systems. In AD, skin inflammation is caused by host–environment interactions involving keratinocytes as well as tissue-resident immune cells such as type 2 innate lymphoid cells, basophils, mast cells, and T helper type 2 cells, which produce type 2 cytokines, including IL-4, IL-5, IL-13, and IL-31. Type 2 inflammation broadly impacts the expression of genes relevant for barrier function, such as intracellular structural proteins, extracellular lipids, and junctional proteins, and enhances Staphylococcus aureus skin colonization.A Human Skin Model for Assessing Arboviral Infections
Arboviruses such as flaviviruses and alphaviruses cause a significant human healthcare burden on a global scale. Transmission of these viruses occurs during human blood feeding at the mosquito-skin interface. Not only do pathogen immune evasion strategies influence the initial infection and replication of pathogens delivered, but arthropod salivary factors also influence transmission foci. In vitro cell cultures do not provide an adequate environment to study complex interactions between viral, mosquito, and host factors.
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